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PubMed1982

Etomidate-analgesic combinations for the induction of anaesthesia in cardiac patients. Part I: Studies in patients with coronary artery disease.

UNLABELLED: In a total of 150 patients undergoing coronary revascularization procedures etomidate was given for the induction of anaesthesia using 12 different dosages and combinations with piritramide, morphine, fentanyl and nitrous oxide. The aim of this study was to establish a method which would result in the smallest possible changes in arterial blood pressure and heart rate during the whole of the induction period, including the stressful phase of endotracheal intubation. In 68 patients cardiac output and pulmonary artery pressure were also measured. RESULTS: 1. In general, more favourable results were obtained when anaesthetic drugs were administered extremely slowly (e.g. by infusion) and according to a standardized dosetime regime. Conversely, the commonly used method - slow incremental injections according to the estimated requirements of the individual patient - led to much greater variations of arterial pressure, especially when fentanyl was combined with etomidate. 2. Combinations of etomidate and morphine led to unsatisfactory results. Dependent on the dose given, hypertension or hypotension were commonly seen. When piritramide was substituted for morphine much more stable haemodynamic conditions were obtained. 3. Surveying our investigations to find the most suitable dose relationship between the hypnotic, etomidate, and the opioid analgesic, piritramide, only small and negligible differences were found: comparing two procedures for the induction of anaesthesia using either high dose piritramide (3 mg . kg-1 given over 10 min), supplemented by low dose etomidate (0.1 mg . kg-1 given over the first 2 min) or an etomidate infusion (50 gamma . kg-1 . min-1) supplemented by a low dose piritramide (0.3 mg . kg-1 given over 1 min) excellent results were found in both groups. 4. In contrast, studies aimed at achieving equally favourable results using the combination of etomidate-fentanyl suggested that the safe dose-range of fentanyl is very narrow: etomidate-infusion (50 gamma . kg-1 . min-1) together with fentanyl 3 gamma . kg-1 led to unacceptable rises in blood pressure and heart rate after intubation, and the larger dose of 6 gamma . kg-1 fentanyl frequently led to hypotension.

Analgesics↗
PubMed1994

Acute toxicosis in two dogs associated with etomidate-propylene glycol infusion.

Etomidate, formulated in propylene glycol, was used as the primary anesthetic agent in two dogs (No. 1 and 2) and etomidate, formulated in saline, was used as the primary anesthetic agent in an additional 20 dogs, while developing a canine model for baroreceptor sensitivity testing. Dogs 1 and 2 had signs of acute toxicosis after infusion of etomidate in propylene glycol. Dog 1 received less total etomidate than did dog 2, 5.9 mg/kg vs 15.8 mg/kg, respectively. Average infusion rates were 4.7 and 9 mg/kg/h, respectively. Dog 1 developed clinical signs of mild hemoglobinuria, whereas dog 2 recovered from anesthesia slowly, was obtunded, bradycardic, and hypothermic, with marked hemoglobinuria and intravascular hemolysis. After supportive treatment, dog 2 regained consciousness and hemodynamic variables improved within 12 h. None of the additional 20 dogs that received infusion of etomidate in saline had any clinical adverse effects, suggesting a causal relationship between the etomidate-propylene glycol formulation and the adverse effects in dogs 1 and 2. Although etomidate may be useful in designing cardiovascular models under general anesthesia, such complications may warrant use of a different etomidate formulation in the dog when the agent is administered at these infusion rates.

Anesthesia, General↗
PubMed1993

[Comparative effectiveness and tolerance study of a new galenic etomidate formula].

OBJECTIVE AND STUDY DESIGN: One of the major disadvantages of etomidate is the high frequency of pain on injection. A new galenic formulation based on a lipid emulsion for etomidate (Etomidat-Lipuro) was compared with the commercial standard (etomidate in propylene glycol, Hypnomidate) in a prospective, randomised, double-blind clinical evaluation in 232 patients undergoing elective surgery in general anaesthesia. The patients were premedicated with flunitrazepam 2 hours before the investigation. Two intravenous cannulas were inserted in veins of forearm or back of the hand. One cannula was only used for the application of etomidate and removed immediately after injection. General anaesthesia was induced with 0.3 mg/kg etomidate at an injection rate of 20 mg/30 s. If the patient did not complain of pain or other sensations during injection spontaneously, he was questioned for 15 s after beginning of injection. The arm used for application of etomidate was kept free of any manipulation during the operation and the following five postoperative days. RESULTS: There were marked differences between the two etomidate preparations concerning venous irritation. About 20% of the patients receiving the hypnotic in propylene glycol complained spontaneously of pain on injection, whereas none with the lipid emulsion. No difference was found in the incidence of myoclonic movements. The time interval between the beginning of injection and loss of eyelid closure reflex was about 50 s and not different for the two galenic formulations. Blood pressure during and after induction of anaesthesia did not differ. The heart rate in the group of patients with etomidate in lipid emulsion was slightly increased before and immediately after intubation compared to the propylene glycol group. 4% of the patients in the propylene glycol group suffered from postoperative venous complications as reddening, swelling, induration or pain. These complications could not be seen in the lipid emulsion group.

Adult↗
PubMed2006

Effect of propofol and etomidate on normoxic and chronically hypoxic pulmonary artery.

BACKGROUND: Chronic alveolar hypoxia results in sustained arterial constriction, and increase in pulmonary vascular resistance leading to pulmonary artery hypertension (PAHT). The aim of this study was to investigate the effect of propofol and etomidate on pulmonary artery (PA) reactivity in chronically hypoxic (CH) rats, a model of pulmonary arterial hypertension (PAHT), in normoxic animals, and human PA. METHODS: CH rats were maintained 14 days at 380 mmHg pressure in a hypobaric chamber. Human tissue was retrieved from histological lung pieces from patients undergoing resection for carcinoma. Cumulative concentrations of anaesthetics were tested on isolated vascular rings precontracted with phenylephrine (PHE) or 100 mM KCl. Statistical comparisons were done by ANOVA, followed, when needed, by Student t tests with Bonferroni correction as post-hoc tests. RESULTS: In normoxic rat PA, maximal relaxation (Rmax) induced by etomidate and propofol was 101.3 +/- 0.8% and 94.0 +/- 2.3%, respectively, in KCl-precontracted rings, and 63.3 +/- 9.7% and 46.1 +/- 9.1%, respectively, in PHE-precontracted rings (n = 7). In KCl-precontracted human PA, Rmax was 84.7 +/- 8.6 % and 66.5 +/- 11.8%, for etomidate and propofol, respectively, and 154.2 +/- 22.4 % and 51.6 +/- 15.1 %, respectively, in PHE-precontracted human PA (n = 7). In CH rat PA, the relaxant effect of both anaesthetics was increased in PHE-precontracted and, for etomidate only, in KCl-precontracted PA. In aorta, CH induced no change in the relaxant effect of anaesthetics. CONCLUSION: Propofol and etomidate have relaxant properties in PA from human and normoxic rat. The relaxant effect is specifically accentuated in PA from CH rat, mainly via an effect on the pharmacomechanical coupling. Etomidate appears to be more efficient than propofol at identical concentration, but, taking into account clinical concentrations, etomidate is less potent than propofol, which effect was in the range of clinical doses. Although these findings provide experimental support for the preferential use of etomidate for haemodynamic stability in patients suffering from PAHT, the clinical relevance of the observations requires further investigation.

Journal Article↗
PubMed1976

The plasma protein binding and distribution of etomidate in dog, rat and human blood.

The interactions of etomidate and its major metabolite (R 28 141) with plasma proteins were studied by equilibrium dialysis with a multiple cell system. A 4% human serum albumin solution was able to bind 78.5% of the etomidate, and 60.5% of R 25 141, whereas a 1.5% human gamma globulin solution bound etomidate for not more than 3% and did not bind R 28 141 at all. The association constants and free binding energies for the binding of etomidate and R 28 141 to human serum albumin were determined. Plasma protein binding of etomidate was 75.4% in the dog and 76.5% in man; in rat plasma 79.5% of the radioactivity was bound to the plasma proteins, however the etomidate was partly hydrolyzed, even in the presence of sodium fluoride. In the rat 29.7% was distributed to the blood cells, 55.9% bound to plasma proteins and 14.4% was present in plasma water; in the dog the distribution percentages were 42.1%, 43.7% and 14.2% respectively, and in man 37.7%, 47.6% and 14.7% respectively. The major metabolite of etomidate was distributed for 26.3% to the human blood cells, 47.4% was bound to plasma proteins and 26.2% was present in the plasma water; its plasma protein binding amounted to 64.3%. Etomidate was bound at or in the blood cells, whereas R 28 141 was not.

Blood Proteins↗
PubMed2004

In vitro and in vivo evaluation of a sulfobutyl ether beta-cyclodextrin enabled etomidate formulation.

In this study, we report the formulation and in vivo evaluation of etomidate in an aqueous solution using sulfobutyl ether-7 beta-cyclodextrin (SBE-CD, Captisol) as a solubilizing agent. The phase-solubility behavior of etomidate as a function of SBE-CD concentration was evaluated, and accelerated solution stability studies of 2 mg/mL etomidate in a 5% w/v SBE-CD solution were conducted. The intravenous administration of the SBE-CD etomidate formulation in dogs was compared with Amidate, the commercial etomidate drug product formulated with propylene glycol as a cosolvent. The etomidate plasma concentration-time data were fit to a three-compartment mamillary model and the derived standard pharmacokinetic parameters were not statistically different between the two formulations (n = 4, p > 0.050). Concurrent pharmacodynamic analysis provided statistically equivalent maximum effects and median inhibitory concentrations for the two formulations. In vivo hemolysis after intravenous administration of Amidate was 10-fold higher than the SBE-CD formulation. Whereas Amidate cannot be given subcutaneously because of the cosolvent in the formulation, a 12 mg/mL aqueous solution of etomidate in 20% (w/v) SBE-CD was well tolerated by this route. The results suggest that the SBE-CD formulation is a viable clinical drug product with a reduced side-effect profile.

Adjuvants, Pharmaceutic↗
PubMed1983

The use of etomidate in the management of severe head injury.

The effects of continuous and supplementary bolus dose administration of etomidate have been investigated in ten artificially ventilated patients in traumatic coma. Continuous infusion of etomidate (5-25 micrograms/kg/min) proved to be a practical and safe means of sedating these patients and appeared to control moderately elevated ICP. Additional bolus doses of etomidate (0.2 mg/kg) always reduced acutely elevated ICP (greater than 20 mmHg), which fell by a mean of 33%. However, MAP usually fell, and occasionally serious hypotension occurred. Of a total of 61 bolus dose administrations which were analysed, CPP rose on 40 occasions, fell on 19 and was unchanged twice. There was a weak correlation between the control level of ICP and the magnitude of the fall in ICP in response to the bolus dose of etomidate (r = 0.51, p less than 0.001). Bolus doses of etomidate given just before noxious stimulation, for example chest physiotherapy, prevented or limited the expected rise in ICP (with bolus mean change in ICP = -2.7 +/- 6.9 mmHg, without bolus mean change in ICP = +7.0 +/- 6.4 mmHg). Again MAP tended to fall following the bolus dose. Overall CPP tended to fall slightly following stimulation whether or not a bolus dose was administered (-3.2 +/- 11.1 mmHg and -4.9 +/- 11.5 mmHg respectively). However, when the bolus of etomidate was not given, occasional dramatic and dangerous rises in ICP were seen, in spite of the infusion, during which CPP fell to critical levels. This very rarely occurred when the bolus had been given. Furthermore, serious episodes of hypotension in response to etomidate administration appeared to occur mainly in patients who were relatively hypo-volaemic.

Adolescent↗
PubMed1984

Etomidate: a selective adrenocortical 11 beta-hydroxylase inhibitor.

To investigate the adrenocortical suppression caused by the anesthetic etomidate, plasma levels of progesterone (P), 17-hydroxyprogesterone (17-OHP), 11-deoxycorticosterone (DOC), corticosterone (B), aldosterone (Aldo), 11-deoxycortisol (S), cortisol (F), and cortisone (E) were measured simultaneously before and after a short-term ACTH stimulation test in a 6.5-year-old boy whose convulsions could be kept under control only with constant etomidate infusions. During etomidate therapy, plasma levels of DOC and S were extremely elevated, the progestins P and 17-OHP were slightly elevated, whereas B and Aldo were in the lower normal range, and F and E were markedly decreased. A short-term ACTH stimulation test during etomidate infusion gave a blunted response of B, Aldo, F and E, whereas the level of DOC remained high and S even further increased. P and 17-OHP showed a positive response to ACTH. The ratios of B/DOC and F/S, which reflect adrenocortical 11 beta-hydroxylase activity, were extremely decreased during etomidate and did not change after ACTH stimulation. In contrast, the ratios of DOC/P and S/17-OHP, which reflect 21-hydroxylase activity, were elevated and remained elevated after ACTH stimulation. After discontinuation of etomidate therapy, all the baseline steroid levels were somewhat elevated, but responded normally to ACTH. These results demonstrate that etomidate causes a specific and reversible blockade of the 11 beta-hydroxylation of adrenal steroid synthesis.

17-alpha-Hydroxyprogesterone↗
PubMed1988

Nonhypnotic low-dose etomidate for rapid correction of hypercortisolaemia in Cushing's syndrome.

We determined the adrenostatic potential of low-dose nonhypnotic etomidate in six patients with Cushing's syndrome (ectopic Cushing's syndrome, n = 2; Cushing's disease, n = 3; bilateral adrenal adenoma, n = 1). Etomidate was given as a continuous infusion for 32 h in a dose of 2.5 mg/h (n = 5) or 0.3 mg/kg/h (n = 3), respectively. Saline was given during a control period. The responsiveness to exogenous ACTH was studied during placebo and 7 and 31 h after commencing etomidate by administration of 250 micrograms 1-24 ACTH i.v. Etomidate (2.5 mg/h) led to a consistent decrease in serum cortisol in all patients from a mean of 39.4 +/- 13.3 to 21.1 +/- 5.7 micrograms/dl after 7 h (P less than 0.05 compared with placebo). After 24 h cortisol was reduced further to a mean steady state concentration of 12.3 +/- 5.7 micrograms/dl (P less than 0.05). At the end of the infusion period the cortisol increase in response to ACTH was reduced but not abolished. In contrast, a dose of 0.3 mg/kg/h etomidate induced unresponsiveness of serum cortisol to exogenous ACTH within 7 h. However, sedation was observed in two out of three patients at this dose, while during etomidate in a dose of 2.5 mg/h no side effects were seen. We conclude that low-dose nonhypnotic etomidate reduces serum cortisol to within the normal range in patients with Cushing's syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Neuroprotective effect of etomidate in the central nervous system of streptozotocin-induced diabetic rats.

It is well known that hyperglycaemia due to diabetes mellitus leads to oxidative stress in the central nervous system. Oxidative stress plays important role in the pathogenesis of neurodegenerative changes. In the present study we investigated the possible neuroprotective effect of etomidate against streptozotocin-induced (STZ-induced) hyperglycaemia in the rat brain and spinal cord. A total of 40 rats were used in this study. Rats were divided into four groups: sham-control, diabetic, diabetic-etomidate treated and vehicle for etomidate treatment group. Diabetes mellitus was induced by a single injection of streptozotocin (60 mg/kg body weight). Three days after streptozotocin injection, etomidate (2 mg/kg) was injected intraperitoneally for etomidate group and lipid emulsion (10%) for vehicle group was injected with corresponding amount intraperitoneally every day for 6 weeks. Six weeks after streptozotocin injection, seven rats from each group were killed and brain, brain stem and cervical spinal cord were removed. The hippocampus, cortex, cerebellum, brain stem and spinal cord were dissected for the biochemical analysis (the level of malondialdehyde [MDA], total nitrite, reduced glutathione [GSH], and xanthine oxidase [XO] activity). STZ-induced diabetes resulted in significantly elevation of MDA, XO and nitrite levels in the hippocampus, cortex, cerebellum, brain stem and spinal cord of the rats (P < 0.05) while etomidate treatment provided significantly lower values (P < 0.05). This study demonstrated that etomidate have neuroprotective effect on the neuronal tissue against the diabetic oxidative damage.

Animals↗
PubMed2005

Etomidate and midazolam for procedural sedation: prospective, randomized trial.

OBJECTIVE: To evaluate whether there is a difference in the time of sedation and time to patient disposition in patients undergoing procedural sedation with etomidate and midazolam. METHODS: Prospective, randomized, double-blind trial comparing etomidate (0.10 mg/kg) and midazolam (0.035 mg/kg) for patients requiring procedural sedation for reduction of joint dislocations or long bone fractures. RESULTS: Forty-five patients were enrolled (24 randomized to etomidate, 21 to midazolam). Groups were similar in demographics and analgesic dosing. Mean time of sedation for etomidate was 15 minutes (SD, 10.97) and for midazolam was 32 minutes (SD, 16.13) (P<.001). Mean time to disposition for etomidate was 121 minutes (SD, 73.28) and for midazolam was 111 minutes (SD, 96.36) (P=.700). The mean quality of sedation for etomidate was 7.91 (SD, 1.53) and for midazolam was 7.48 (SD, 2.89) (P=.570). CONCLUSIONS: The use of etomidate compared with midazolam for procedural sedation provides a significant reduction in recovery time, without a reduction in time to patient disposition, while providing equal sedation quality.

Adult↗
PubMed2006

Etomidate versus midazolam for out-of-hospital intubation: a prospective, randomized trial.

STUDY OBJECTIVE: The primary objective of this study is to compare the intubation success rates of etomidate and midazolam when used for sedative-facilitated intubation, without paralytics, in out-of-hospital adult patients. METHODS: This prospective, double-blind, randomized trial was conducted with 2 ground out-of-hospital advanced life support systems (ALS); all patients aged 18 or older who required out-of-hospital sedative-facilitated intubation were eligible for participation. The ambulances were stocked with blinded numbered syringes containing either 7 mg of midazolam or 20 mg of etomidate. No paralytics were used. If sedation was not achieved with the study drug, medics could request additional sedation from a medical command physician; only midazolam or diazepam were available outside of the study. RESULTS: One hundred ten patients were enrolled in the study; 55 patients received midazolam and 55 patients received etomidate. The 2 groups were similar with regard to age, sex, initial vital signs, and reasons for intubation or sedation. The overall intubation success rate was 76% (95% confidence interval [CI] 68% to 84%); 75% (41/55) for midazolam (95% CI 64% to 86%) and 76% (42/55) for etomidate (95% CI 65% to 87%). There was also no difference in incidence of hypotension, number of intubation attempts, or perceived difficulty of intubation. Additional sedation was requested almost equally for the 2 groups: 14 patients in the midazolam group and 12 patients in the etomidate group. A benzodiazepine was successful for rescue of a failed etomidate intubation 10 of 12 times (83%; 95% CI 62% to 100%). When used for rescue of failed midazolam intubations, benzodiazepines were effective in only 5 of 14 (36%, 95% CI 11% to 61%) attempts. CONCLUSION: There were no observed differences between midazolam and etomidate in sedation-facilitated intubation success rates; we could not fully evaluate global outcomes of these agents or the sedative-facilitated intubation strategy itself.

Adolescent↗
PubMed2006

[Prevention of myoclonus after etomidate using a priming dose].

OBJECTIVE: To investigate the influence of pretreatment with a low dose of etomidate (priming dose) on the incidence of etomidate-induced myoclonus. STUDY DESIGN: Prospective randomized double-blind study. METHODS: Forty six patients ASA physical status I - II, scheduled for abdominal elective surgery, were allocated randomly to receive either pre-treatment 0.03 mg/kg of etomidate (priming group) or placebo (control group). Sixty-seconds after the pre-treatment was injected, anesthesia was induced with etomidate 0.3 mg/kg and 60 seconds later induction was completed with fentanyl (3 microg/kg) and vecuronium (0.1 mg/kg). The occurrence and intensity of myoclonus were graded clinically by a blinded observer as: 0=no myoclonus, 1=mild myoclonus, 2=moderate myoclonus and 3=severe myoclonus. STATISTICAL ANALYSIS: Fisher test exact for qualitative variable and Student t-test for quantitative variables. RESULTS: Demographic data and the average dose of etomidate used during the induction were similar in the 2 groups (0.29+/-0.032 mg/kg in the priming group and 0.30+/-0.029 mg/kg in the control group). Twenty patients (87%) in the control group experienced myoclonic movements whereas only 6 patients (26%) in the control group had such movements (P<0,001). CONCLUSION: Pretreatment with etomidate (0.03 mg/kg), given 60 seconds before induction of anesthesia, is effective at reducing etomidate-induced myoclonus, without related side-effect.

Aged↗
PubMed2002

Comparison of the effects of remifentanil or fentanyl on anaesthetic induction characteristics of propofol, thiopental or etomidate.

BACKGROUND AND OBJECTIVE: This prospective, randomized, double-blinded study was designed to compare the effects of remifentanil or fentanyl on anaesthetic induction characteristics of propofol, thiopental or etomidate. METHODS: Seventy-two patients were enrolled in six groups of 12 individuals each. In three groups, fentanyl was given as a bolus dose of 1.5 microg kg(-1), whereas the others received a remifentanil infusion at 0.5 microg kg(-1) min(-1). Five minutes later, propofol, thiopental or etomidate were titrated to a state of unresponsiveness. Assessment included the amounts of drug necessary for induction, haemodynamics and the times to apnoea, loss of eyelash reflex, and the release of a water-filled syringe held in the patient's hand. RESULTS: Induction times to loss of the eyelash reflex were significantly shorter in the remifentanil than in the fentanyl groups: with propofol 50.7 +/- 13.6s (mean +/- SD) versus 74.9 +/- 27.0s (P < 0.01), with thiopental 42.9 +/- 16.8s versus 77.2 +/- 27.8s (P < 0.01) and with etomidate 54.7 +/- 17.6s versus 72.3 +/- 24.0s (P < 0.05). The times to respiratory arrest or for the syringe to fall were significantly shorter with remifentanil than with fentanyl for propofol and for thiopental, but not for etomidate. In terms of dosages per kg body weight necessary to achieve unresponsiveness, less propofol (-29%, P < 0.05), thiopental (-25%, P < 0.05) or etomidate (-32%, P < 0.01) was necessary with remifentanil than with fentanyl. Haemodynamic responses to tracheal intubation were controlled more effectively with remifentanil. However, within the remifentanil groups, mean arterial pressure significantly decreased during induction: -26% with propofol, -181% with thiopental and -14% with etomidate (all P < 0.01). CONCLUSIONS: During anaesthetic induction, a remifentanil infusion of 0.5 microg kg(-1) min(-1) over 5 min is a suitable alternative to a 1.5 microg kg(-1) bolus dose of fentanyl: induction times are shorter with reduced amounts of propofol, thiopental or etomidate.

Adult↗
PubMed1997

Cerebral hypoxia after etomidate administration and temporary cerebral artery occlusion.

UNLABELLED: Neurovascular surgical procedures often require temporary cerebral arterial occlusion. Although clinical validation is lacking, etomidate has often been used to attenuate the effects of cerebral ischemia in this setting. The purpose of this study was to evaluate the effects of etomidate and temporary cerebral arterial occlusion on human brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH during intracranial aneurysm surgery. We studied nine patients presenting for cerebral aneurysm surgery. A Paratrend probe was used to determine brain tissue pH and gas tensions. Etomidate was administered to produce electroencephalographic burst suppression before temporary cerebral arterial occlusion. After etomidate administration in nine patients, brain tissue PO2 decreased 30% compared with baseline (P < 0.05). During temporary brain artery occlusion in 8 patients, tissue PO2 decreased 32% below preclip values (P < 0.05) in conjunction with a tissue PCO2 increase of 23% (P < 0.05) and a 0.1-unit decrease in pH (P < 0.05). In patients in whom PO2 decreased below 10 mm Hg during temporary clipping, tissue pH decreased, compared with patients in whom PO2 remained above 10 mm Hg (P < 0.05). These results demonstrate that etomidate administration during cerebral aneurysm surgery decreases tissue PO2 and that in these patients, tissue PO2 does not increase with increases in inspired oxygen concentration. Low tissue PO2 during temporary clipping significantly increases the risk of tissue acidosis. IMPLICATIONS: Etomidate administration alone resulted in cerebral deoxygenation. Subsequent temporary cerebral artery occlusion resulted in additional tissue deoxygenation and acidosis. These results suggest that etomidate enhances hypoxic risk in the setting of cerebral ischemia.

Adult↗
PubMed1985

Comparison of the ventilatory effects of etomidate and methohexital.

Using a dual-isohypercapnic technique, the authors determined the effect of equipotent doses of methohexital (1.5 mg/kg) and etomidate (0.3 mg/kg) on the ventilatory response to CO2 (VERCO2) in six healthy volunteers. Speed of induction and duration of hypnosis did not differ significantly between the two drugs. Within 2 min after injection, the slope of VERCO2 decreased significantly after both methohexital (from 2.52 to a minimum of 0.15 l . min-1 . mmHg-1, P less than 0.05) and etomidate (from 2.56 to a minimum of 0.62 l . min-1 . mmHg-1, P less than 0.05); the magnitude of this depression did not differ significantly between the drugs. Methohexital also caused a significant decrease in minute ventilation at end-tidal PCO2 of 46 mmHg (VE 46) from 14.6 to 4.3 l . min-1 within 60 s after injection (P less than 0.05). In contrast, after etomidate VE 46 gradually increased from 17.9 1 . min-1 to a maximum of 31.6 l . min-1 at 3.5 min after injection (P less than 0.05); respiratory rate increased significantly, while changes in tidal volume were not significant. Effects of etomidate and methohexital on VE 46 differed significantly (P less than 0.001). These data indicate that, while etomidate and methohexital similarly depress the medullary centers that modify ventilatory drive in response to changing CO2 tensions, ventilation at any given CO2 tension is greater after etomidate than after methohexital. This indicates that etomidate may cause a CO2-independent stimulation of ventilation, suggesting its use for induction of anesthesia in cases where maintenance of spontaneous ventilation is desirable.

Adult↗
PubMed1988

Effect of etomidate on hepatic drug metabolism in humans.

The authors studied the effect of etomidate on drug metabolism in vivo in humans and in vitro using human liver microsomes. When these liver microsomes were incubated with different concentrations of etomidate, dose-dependent inhibition of ketamine N-demethylation, a cytochrome P-450-dependent enzymatic process, was produced. Cytochrome P-450 binding spectra displayed type II binding with a UV light absorption maximum (lambda max) at a wavelength of 424 nm in the presence of etomidate. In vivo studies were conducted using ketamine and antipyrine as substrates. Evaluation of antipyrine's pharmacokinetic variables after an intravenous infusion of etomidate (0.34 +/- 0.17 mg/kg) revealed an 18% increase in its elimination half-life (P = 0.04). In addition, there were 16% and 11% decreases in the area under the curve (P = 0.05) and in the clearance rate (P = 0.07) for antipyrine, respectively. In patients administered a bolus dose of ketamine during brief outpatient operations, etomidate produced no significant changes in ketamine's pharmacokinetics compared to thiopental. The authors conclude that the etomidate-induced inhibition of hepatic drug metabolism can prolong the elimination of drugs with low hepatic clearance rates (e.g., antipyrine). However, etomidate would not be expected to alter the rate of elimination of high clearance anesthetics and analgesic drugs (e.g., ketamine, fentanyl).

Antipyrine↗
PubMed1996

Comparison of the effects of etomidate, propofol, and thiopental on respiratory resistance after tracheal intubation.

BACKGROUND: Tracheal intubation frequently results in reversible bronchoconstriction. Propofol has been reported to minimize this response in healthy patients and in asthma patients, but may be unsuitable for hemodynamically unstable patients for whom etomidate may be preferable. The current study examined respiratory resistance after tracheal intubation after induction with either thiopental, etomidate, or propofol. A supratherapeutic dose of etomidate was used to test the hypothesis that the bronchoconstrictive response could be minimized by deep intravenous anesthesia. METHODS: Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction. RESULTS: Respiratory resistance at 2 min was 8.1 +/- 3.4 cmH2O.1(-1).s (mean +/- SD) for patients receiving propofol versus 11.3 +/- 5.3 for patients receiving etomidate and 12.3 +/- 7.9 for patients receiving thiopental (P < or = 0.05 for propofol vs. either etomidate or thiopental). CONCLUSIONS: Respiratory resistance after tracheal intubation is lower after induction with propofol than after induction with thiopental or after induction with high-dose etomidate.

Adult↗